Medicine, via pristina

Medicine, via pristina

Asystole 

1. Knuuti J, Wijns W, Saraste A, Capodanno D, Barbato E, Funck-Brentano C, et al. 2019 ESC Guidelines for the diagnosis and management of chronic coronary syndromes. Eur Heart J. 2020;41(3):407-477.
PMID: 31504439
DOI: https://doi.org/10.1093/eurheartj/ehz425


2. Fihn SD, Gardin JM, Abrams J, Berra K, Blankenship JC, Dallas AP, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease. J Am Coll Cardiol. 2012;60(24):e44-e164.
PMID: 23182125
DOI: https://doi.org/10.1016/j.jacc.2012.07.013


3. Khan MA, Hashim MJ, Mustafa H, Baniyas MY, Al Suwaidi SKBM, AlKatheeri R, et al. Global epidemiology of ischemic heart disease: Results from the Global Burden of Disease Study. Cureus. 2020;12(7):e9349.
PMID: 32742886
DOI: 10.7759/cureus.9349


4. Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2018;39(2):119-177.
PMID: 28886621
DOI: https://doi.org/10.1093/eurheartj/ehx393


5. Amsterdam EA, Wenger NK, Brindis RG, Casey DE Jr, Ganiats TG, Holmes DR Jr, et al. 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes. J Am Coll Cardiol. 2014;64(24):e139-e228.
PMID: 25260716
DOI: https://doi.org/10.1016/j.jacc.2014.09.017

Background 

Asystole, also known as “flatline,” is a state of complete absence of ventricular electrical activity, resulting in no cardiac output and no pulse. It is a form of pulseless electrical activity (PEA) and represents one of the non-shockable rhythms in cardiac arrest. Without prompt identification and management, asystole is rapidly fatal. 


II) Classification/Types
 

By Rhythm Status: 

  • True asystole: Complete absence of electrical activity across the myocardium. 
  • Pseudo-asystole: Apparent flatline due to technical issues (e.g., lead disconnection, artifact) or very fine ventricular fibrillation. 

By Underlying Mechanism: 

  • Primary asystole: Resulting from intrinsic failure of the cardiac conduction system. 
  • Secondary asystole: Due to severe metabolic, toxic, or ischemic insult suppressing myocardial activity. 

 

Pathophysiology 

Asystole results from the failure of impulse generation in the sinoatrial node and/or impulse conduction through the myocardium. It may follow a prolonged bradyarrhythmia or PEA. The myocardium becomes electrically and mechanically unresponsive, either due to extensive ischemia, severe electrolyte derangement, profound acidosis, or drug toxicity. 

 

Epidemiology 

  • Common final event in in-hospital and out-of-hospital cardiac arrests 
  • Represents up to 30–40% of non-traumatic adult cardiac arrests 
  • Very poor prognosis compared to shockable rhythms (e.g., VF/pVT) 

 


Etiology
 

I) Causes 

  • Hypoxia 
  • Hypovolemia 
  • Hydrogen ion (acidosis) 
  • Hyper-/hypokalemia 
  • Hypothermia 
  • Tension pneumothorax 
  • Tamponade (cardiac) 
  • Toxins (e.g., opioids, TCA, digoxin) 
  • Thrombosis (pulmonary or coronary) 
  • Trauma (severe hemorrhagic shock) 


II) Risk Factors
 

  • Advanced age 
  • Structural heart disease (e.g., heart failure, MI history) 
  • Chronic kidney disease (prone to hyperkalemia) 
  • Drug overdose or polypharmacy 
  • Recent cardiac surgery 
  • Electrolyte imbalances or acid-base disturbances 

 


Clinical Presentation
 

I) History (Symptoms) 

Often preceded by symptoms of bradycardia or cardiac instability: 

  • Syncope or sudden collapse 
  • Lightheadedness or dizziness 
  • Chest discomfort 
  • Dyspnea or palpitations 
  • Seizure-like activity (due to cerebral hypoperfusion) 


II) Physical Exam (Signs)
 

  • No pulse 
  • Unconscious, unresponsive 
  • No heart sounds 
  • Apnea 
  • Cyanosis or pallor 
  • Cardiac monitor showing flatline or near-flatline 

 


Differential Diagnosis (DDx)
 

  • Fine ventricular fibrillation 
  • Severe bradycardia or PEA 
  • Equipment malfunction or lead disconnection 
  • Profound hypothermia 
  • High-grade AV block without escape rhythm 

 


Diagnostic Tests
 

Initial Work-Up 

  • Cardiac monitor/ECG: Confirm true asystole (check leads and gain) 
  • Pulse check: No palpable pulse 
  • ABG/VBG: Assess for severe acidosis or hypoxia 
  • Electrolytes and glucose: Identify correctable causes 
  • Toxicology screen: If drug overdose suspected 
  • Bedside ultrasound: Rule out tamponade or massive PE 


Advanced Testing
 

(Not performed during arrest but post-resuscitation if ROSC achieved) 

  • Cardiac biomarkers 
  • CT chest or pulmonary angiogram (if PE suspected) 
  • Echocardiogram for structural evaluation 

 


Treatment
 

I) Acute Management (During Cardiac Arrest) 

Follow Advanced Cardiac Life Support (ACLS) for Asystole

  • CPR: High-quality compressions at 100–120/min with minimal interruption 
  • Epinephrine: 1 mg IV/IO every 3–5 minutes 
  • Airway management: Bag-valve-mask ventilation or advanced airway 
  • Identify and treat reversible causes (the H’s and T’s) 
  • DO NOT DEFIBRILLATE: Asystole is non-shockable 
  • Reassess rhythm every 2 minutes 


II) Post-Resuscitation (If ROSC achieved)
 

  • Manage underlying cause (e.g., correct hyperkalemia, initiate antibiotics for sepsis) 
  • Hemodynamic support (vasopressors, fluids) 
  • Targeted temperature management if comatose 
  • Intensive care monitoring 

 

Medications 

Drug Class 

Examples 

Notes 

Vasopressors 

Epinephrine 

Main pharmacologic intervention during asystole 

Buffer agents 

Sodium bicarbonate 

Consider in severe acidosis or known TCA overdose 

Electrolyte agents 

Calcium, insulin/glucose 

For hyperkalemia management 

Antidotes 

Naloxone, digoxin Fab 

For opioid or digoxin toxicity 

Antiarrhythmics 

Not indicated 

Asystole is not responsive to antiarrhythmics 

 

Device Therapy 

  • Temporary pacing: Rarely useful in true asystole unless known high-degree AV block with reversible etiology 
  • Defibrillation: Not indicated in asystole 
  • ECMO: Considered in select centers for refractory cardiac arrest (eCPR) 

 


Patient Education, Screening, Vaccines
 

Education (Post-Recovery, if applicable) 

  • Discuss resuscitation preferences and advance directives 
  • Risk factor modification (e.g., medication review, K⁺ control) 
  • Educate on warning signs of bradyarrhythmias 


Screening/Prevention
 

  • Monitor electrolyte and drug levels in high-risk patients 
  • Regular ECG in patients with conduction disease or on nodal blockers 
  • Avoid QT-prolonging or bradycardia-inducing drugs without indication 


Vaccinations
 

  • None specific to asystole 
  • Routine adult immunizations encouraged (e.g., influenza, pneumococcus) 

 


Consults/Referrals
 

  • Cardiology: For post-resuscitation arrhythmia evaluation 
  • Electrophysiology: For pacemaker consideration in advanced AV block 
  • Critical Care: For post-arrest management 
  • Nephrology: For electrolyte imbalance or dialysis needs 
  • Toxicology: In suspected poisoning or overdose 

 


Follow-Up
 

Short-Term 

  • Monitor for organ dysfunction (e.g., AKI, anoxic brain injury) 
  • Reevaluate need for pacing or ICD if conduction system disease suspected 
  • Rehabilitation for post-cardiac arrest syndrome 


Long-Term
 

  • Ongoing cardiology follow-up 
  • Neurological assessment and cognitive evaluation 
  • Advance care planning discussions 

 

Prognosis 

  • Extremely poor in true asystole without rapid ROSC 
  • Worse outcomes compared to VF/pVT cardiac arrest 
  • Prognosis improved with rapid CPR, early epinephrine, and reversible cause identification 
  • Survivors often suffer from significant neurological impairment 
  • If ROSC achieved and underlying cause treated, long-term survival is possible but uncommon 

 

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